Response to UV-C radiation in topo I-deficient carrot cells with low ascorbate levels. (Articolo in rivista)

Type
Label
  • Response to UV-C radiation in topo I-deficient carrot cells with low ascorbate levels. (Articolo in rivista) (literal)
Anno
  • 2010-01-01T00:00:00+01:00 (literal)
Alternative label
  • Balestrazzi A, Locato V, Bottone MG, De Gara L, Biggiogera M, Pellicciari C, Botti S, Di Gesù D, Donà M, Carbonera D. (2010)
    Response to UV-C radiation in topo I-deficient carrot cells with low ascorbate levels.
    in Journal of experimental botany
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Balestrazzi A, Locato V, Bottone MG, De Gara L, Biggiogera M, Pellicciari C, Botti S, Di Gesù D, Donà M, Carbonera D. (literal)
Pagina inizio
  • 575 (literal)
Pagina fine
  • 585 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 61 (literal)
Rivista
Note
  • ISI Web of Science (WOS) (literal)
Titolo
  • Response to UV-C radiation in topo I-deficient carrot cells with low ascorbate levels. (literal)
Abstract
  • In animal cells, recent studies have emphasized the role played by DNA topoisomerase I (topo I) both as a cofactor of DNA repair complexes and/or as a damage sensor. All these functions are still unexplored in plant cells, where information concerning the relationships between DNA damage, PCD induction, and topo I are also limited. The main goal of this study was to investigate the possible responses activated in topo I-depleted plant cells under oxidative stress conditions which induce DNA damage. The carrot (Daucus carota L.) AT1-beta/22 cell line analysed in this study (characterized by an antisense-mediated reduction of top1beta gene expression of approximately 46% in association with a low ascorbate content) was more sensitive to UV-C radiation than the control line, showing consistent cell death and high levels of 8-oxo-dG accumulation. The topo I-depleted cells were also highly susceptible to the cross-linking agent mitomycin C. The death response was associated with a lack of oxidative burst and there were no changes in ascorbate metabolism in response to UV-C treatment. Electron and fluorescence microscopy suggested the presence of three forms of cell death in the UV-C-treated AT1-beta/22 population: necrosis, apoptotic-like PCD, and autophagy. Taken together, the data reported here support a reduced DNA repair capability in carrot topo I-deficient cells while the putative relationship between topo I-depletion and ascorbate impairment is also discussed. (literal)
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